What question did this study set out to answer?

To determine whether chronic activation of AMPK by metformin restores cardiomyocyte autophagy and preserves cardiac function in diabetic OVE26 mice.

May 12, 2011DiabetesOpen Access

Improvement of Cardiac Functions by Chronic Metformin Treatment Is Associated With Enhanced Cardiac Autophagy in Diabetic OVE26 Mice

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Why the study?

Does metformin improve cardiac function and cardiomyocyte autophagy in diabetic OVE26 mice?

Population

OVE26 diabetic mice and cardiac-specific AMPK dominant negative transgenic (DN)-AMPK diabetic mice

Comparison

Metformin for 4 months vs Vehicle

Design

Preclinical

Follow-up

4 months

Authors

ZXZhonglin XieNorthwestern Polytechnical University KLKai LauPrince Charles Hospital BEBonnie EbyWashington University in St. Louis

Discussion

Member takes

Implication

Hypothesis-generating for AMPK-autophagy in diabetic cardiomyopathy models; does not support clinical practice changes pending human trials.

Key Points

To determine whether chronic activation of AMPK by metformin restores cardiomyocyte autophagy and preserves cardiac function in diabetic OVE26 mice.
Treated diabetic OVE26 mice and cardiac-specific dominant-negative AMPK (DN-AMPK) diabetic mice with metformin or vehicle for 4 months.
Assessed cardiac function in vivo and in isolated perfused hearts, alongside cardiomyocyte autophagy, apoptosis, and structural mitochondrial organization.
Diabetic OVE26 mice exhibited significant reductions in AMPK activity and cardiomyocyte autophagy, accompanied by mitochondrial disorganization, accumulated polyubiquitinated proteins, elevated apoptosis, and cardiac dysfunction.
Genetic inhibition of AMPK via DN-AMPK expression further impaired cardiac autophagy, worsened cardiac dysfunction, and increased mortality in diabetic mice.
Chronic metformin therapy significantly enhanced cardiac autophagy and preserved cardiac performance in diabetic OVE26 mice, but these protective effects failed to occur in DN-AMPK diabetic mice.

Structured PICO

Does metformin improve cardiac function and cardiomyocyte autophagy in diabetic OVE26 mice?

Population

OVE26 diabetic mice and cardiac-specific AMPK dominant negative transgenic (DN)-AMPK diabetic mice

Intervention

Metformin for 4 months

Comparator

Vehicle

Outcome

Cardiac autophagy, cardiac functions, and cardiomyocyte apoptosissurrogate

Chronic AMPK activation by metformin prevents diabetic cardiomyopathy by upregulating autophagy activity in diabetic OVE26 mice.

Cite This Study

Xie et al. (2011) studied this question.

synapsesocial.com/papers/6a7dda82603f5e16dd33aaa6 https://doi.org/10.2337/db10-0351

Topics

Echocardiography Cardiomyopathy

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Implication

Hypothesis-generating for AMPK-autophagy in diabetic cardiomyopathy models; does not support clinical practice changes pending human trials.

Improvement of Cardiac Functions by Chronic Metformin Treatment Is Associated With Enhanced Cardiac Autophagy in Diabetic OVE26 Mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Improvement of Cardiac Functions by Chronic Metformin Treatment Is Associated With Enhanced Cardiac Autophagy in Diabetic OVE26 Mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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